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Contact activation products are new potential biomarkers to evaluate the risk of thrombotic events in systemic lupus erythematosus
Uppsala University.
Skåne University Hospital;Lund University.
Skåne University Hospital;Lund University.
Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University. (Linnaeus Ctr Biomat Chem, BMC)ORCID-id: 0000-0001-7888-1571
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2013 (Engelska)Ingår i: Arthritis Research & Therapy, ISSN 1478-6354, E-ISSN 1478-6362, Vol. 15, nr 6, artikel-id R206Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Introduction: Patients with systemic lupus erythematosus (SLE) have persistent platelet activation and an increased risk of thrombotic events, which cannot be accounted for by traditional cardiovascular risk factors. Factor (F)XII has a potentially important role in thrombus formation and is triggered by activated platelets. We therefore asked whether the contact system is involved in inflammation and vascular disease (VD) in SLE. Methods: Fibrin clots were incubated with purified FXII or whole blood, and the activation and regulation of FXII were studied. Plasma from SLE patients with (n = 31) or without (n = 38) previous VD and from matched healthy controls (n = 68) were analyzed for the presence of complexes formed between contact system enzymes and antithrombin (AT) or C1 inhibitor (C1INH) and evaluated with regard to clinical data and laboratory parameters. Results: Fibrin clots elicited FXII activation and acted as co-factors for AT. In clotting plasma, the levels of FXIIa-AT increased, and FXIIa-C1INH decreased. A similar reciprocal relationship existed in SLE patients. FXIIa-AT was elevated in the SLE patients with a history of VD, while the corresponding levels of factor FXIIa-C1INH were significantly decreased. FXIIa-AT correlated strongly with platelet parameters. The odds ratio for VD among the SLE patients was 8.9 if they had low levels of FXIIa-C1INH, 6.1 for those with high levels of FXIIa-AT, and increased to 23.4 for those with both decreased levels of FXIIa-C1INH and increased levels of FXIIa-AT. Conclusions: Activation of FXII is elicited by fibrin during thrombotic reactions in vitro and in vivo, and fibrin acts as a heparin-like co-factor and regulates AT. Patients with SLE had altered levels of FXIIa-serpin complexes, supporting that the contact system is involved in this disease. FXIIa-serpin complexes are strongly associated with previous VD in SLE patients, suggesting that these complexes are potential biomarkers for monitoring and assessing the risk of thrombotic events in SLE.

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2013. Vol. 15, nr 6, artikel-id R206
Nationell ämneskategori
Immunologi
Forskningsämne
Naturvetenskap, Biomedicinsk vetenskap
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URN: urn:nbn:se:lnu:diva-32678DOI: 10.1186/ar4399ISI: 000330628800032Scopus ID: 2-s2.0-84888780786OAI: oai:DiVA.org:lnu-32678DiVA, id: diva2:703609
Tillgänglig från: 2014-03-07 Skapad: 2014-03-07 Senast uppdaterad: 2018-11-16Bibliografiskt granskad

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Nilsson Ekdahl, Kristina

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